Adenosine Preconditioning Reduces Both Pre and Postischemic Arrhythmias in Human Myocardium

Pomerantz, Benjamin J.; Joo, Kyung Sub; Shames, Brian D.; Cleveland, Joseph C.; Banerjee, Anirban; Harken, Alden H.

doi:10.1006/jsre.2000.5889

Cited by 23 publications

(21 citation statements)

References 14 publications

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“…Several advantages of adenosine production have been suggested, including reducing hypertension (Leesar et al, 1997;Antman et al, 2000;Pomerantz et al, 2000). However, in this study we found that despite AMPD1 deficiency, which is observed among heterozygous and mutated homozygous carriers, adenosine has no compensatory effect on the development of hypertension in patients.…”

Section: Discussioncontrasting

confidence: 63%

Association between the C34T polymorphism of the AMPD1 gene and essential hypertension in Malaysian patients

Nemati¹,

Lü²,

Ramachandran³

et al. 2016

Genet. Mol. Res.

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ABSTRACT. The aim of this study was to determine whether C34T, a common polymorphism of the adenosine monophosphate deaminase 1 gene (AMPD1), is associated with essential hypertension (EH). We hypothesize that C34T is associated with the development of EH. A casecontrol design was used for this study. The DNA was extracted using a commercial kit from the whole blood of 200 patients with hypertension and 200 subjects without hypertension from selected Malaysian ethnicities (Malays, Chinese, and Indians). Polymerase chain reaction followed by restriction fragment length polymorphism (PCR-RFLP) and agarose gel electrophoresis were used for genotyping. The C34T gene polymorphism of AMPD1 was significantly associated with EH in the Malaysian subjects (P < 0.0001). The genotype frequencies of CC, CT, and TT were 6%, 79%, and 15%, respectively, among hypertensive subjects, while no TT genotypes were observed in the normotensive subjects. Further, the frequency of hypertension was higher among T allele carriers than C carriers (OD = 9.94; 95%CI = 6.851-14.434). There were significant differences in the systolic blood pressure, diastolic blood pressure, and pulse pressure (P ˂ 0.05) between the normotensive and hypertensive Malaysian subjects; we believe those difference were caused by the C34T polymorphism. For the first time in Malaysia, the current study provides evidence that a common polymorphism of the AMPD1 gene (C34T) is strongly associated with EH.

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Section: Discussioncontrasting

confidence: 63%

Association between the C34T polymorphism of the AMPD1 gene and essential hypertension in Malaysian patients

Nemati¹,

Lü²,

Ramachandran³

et al. 2016

Genet. Mol. Res.

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“…This benefit may be linked to the enhanced production of adenosine since adenosine has cardioprotective actions, including augmentation of coronary blood flow and ischaemic preconditioning [11,12] .…”

Section: Introductionmentioning

confidence: 99%

Association between AMPD1 Gene Polymorphism and Coagulation Factors in Patients with Coronary Heart Disease

Agewall¹,

Norman²

2006

Pathophysiol Haemos Thromb

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The aim of this study was to investigate whether the C34T and G468T variations in the adenosine monophosphate deaminase-1 (AMPD1) gene were associated with intima-media thickness of the carotid and brachial artery, endothelial function of the brachial artery, glucose metabolism, haemostatic variables and cardiac hypertrophy in patients (n = 109) with coronary heart disease. The plasminogen activator inhibitor-1 activity and the von Willebrand factor were higher in the CC homozygote group compared to the CT/TT group (p < 0.05). There were no differences between the groups regarding intima-media complex of the carotid and brachial artery, presence of plaque in the carotid region, flow-mediated dilatation, ejection fraction or dimensions of the heart. In conclusion, there were no differences between the mutant AMPD1 allele carriers and CC homozygotes regarding surrogate values for atherosclerosis, endothelial function, dimensions and ejection fraction of the heart, glucose tolerance and other well-known cardiovascular risk factors, whereas plasminogen activator inhibitor-1 activity and von Willebrand levels were lower in the mutant AMPD1 allele carriers.

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“…Here, I believe, we have an excellent example of the principle proverbially illustrated by the strikingly disparate interpretations of the true nature of an elephant by a group of blind men, each one based upon the limited palpation of a different appendage thereof. Similarly, the somewhat remarkable salutary effects of ischemic preconditioning have been variously attributed to arachidonic acid metabolism (prostaglandins/leukotrienes), 18,19 acidosis, 20 calcium fluxes, 21 reactive oxygen species ("free radicals"), 4,[22][23][24][25] including the currently fashionable nitric oxide free radical, 26 the synthesis of antioxidant enzymes, 27 heat shock protein expression, 28,29 the PARS pathway, 30 apoptosis, 31 purine (adenosine) signaling, 32 kinins, 33,34 glutamate receptors, endothelial adhesion molecule expression, 5,35,36 and a host of intracellular signalling pathways, including tumor necrosis factor, 37 protein kinase C, 38 G-proteins, ceramide, 39 and innumerable others. Indeed, each of the above cited studies does suggest the association of one or more of the above mechanisms with the clinically relevant beneficial effects of ischemic preconditioning.…”

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confidence: 99%

Preconditioning for Protection from Ischemic Injury: Discriminating Cause From Effect From Epiphenomenon

Bulkley¹

2000

Annals of Surgery

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The quest for protection from ischemic (actually ischemia/reperfusion) injury is not new, but in the past several years, this concept has been approached somewhat more rigorously by investigators addressing important clinical problems, particularly heart attack, cardiopulmonary bypass, stroke, peripheral vascular embolism, and the preservation of organs for transplantation. Much of the recent work has focused on the rather remarkable observation that relatively short periods of ischemia sustained just prior to a more prolonged (i.e., clinically relevant) episode appear to have improved the tolerance to the latter in a number of organs, including the heart, brain, 1 spinal cord, 2 skeletal muscle, 3 retina, kidney, intestine, 4 -6 and liver.

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Adenosine Preconditioning Reduces Both Pre and Postischemic Arrhythmias in Human Myocardium

Cited by 23 publications

References 14 publications

Association between the C34T polymorphism of the AMPD1 gene and essential hypertension in Malaysian patients

Association between the C34T polymorphism of the AMPD1 gene and essential hypertension in Malaysian patients

Association between AMPD1 Gene Polymorphism and Coagulation Factors in Patients with Coronary Heart Disease

Preconditioning for Protection from Ischemic Injury: Discriminating Cause From Effect From Epiphenomenon

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